Monopril: instructions for use, analogues, reviews, price

Release form

Monopril is a white, round, biconvex, odorless tablet, scored on one edge and engraved “609” or “158” on the other.

Available according to:

14 such tablets of 20 mg in a blister, two blisters in a paper pack;
10 such tablets of 10 mg each in a blister made of plastic and aluminum foil, one or two blisters in a paper pack;
14 such tablets of 10 mg each in a blister made of plastic and aluminum foil, one or two blisters in a paper pack.

Pharmacodynamics and pharmacokinetics

Pharmacodynamics

Angiotensin-converting enzyme inhibitor. Chemically, fosinopril sodium is the sodium salt of fosinoprilat ester. Fosinoprilat is a selective competitive angiotensin-converting enzyme . After inhibiting ACE, it prevents the transformation of angiotensin type 1 into angiotensin type 2, which has a vasopressor effect. This leads to a decrease in the content angiotensin in the blood - this causes a decrease in its vasoconstrictor activity and a weakening of aldosterone .

Fosinoprilat inhibits the metabolism of bradykinin and therefore its antihypertensive effect is enhanced. The decrease in pressure is not accompanied by a decrease or increase in circulating blood volume, renal and cerebral blood flow, or blood supply to organs. After internal administration, the antihypertensive effect occurs within one hour, becomes maximum after 2-5 hours and lasts up to a day. Several weeks are necessary to achieve the greatest therapeutic effect.

The antihypertensive effects of thiazide diuretics and fosinopril are complementary.

The drug helps reduce sensitivity to physical activity and reduce the severity of heart failure.

Pharmacokinetics

After oral administration, absorption from the intestine reaches 30-40% and does not depend on food intake. Maximum plasma concentration occurs after three hours. Interaction with blood proteins reaches 95%.

Enzymatic hydrolysis of the drug occurs in the liver and intestinal mucosa. Fosinoprilat is excreted equally through the digestive tract and kidneys. The half-life is close to 11 hours.

Pharmacodynamics

Fosinopril is an ester that is hydrolyzed in the body by enzymes into the active compound fosinoprilate. Due to the specific connection of the phosphinate group with ACE, it prevents the conversion of angiotensin I into the vasoconstrictor substance angiotensin II, which leads to vasodilation and a decrease in aldosterone secretion. The latter effect may lead to a slight increase in serum potassium ion concentration (average 0.1 mEq/L) and a decrease in sodium ion concentration and fluid volume. Fosinopril inhibits the metabolism of the bradykinin peptide, which has a powerful vasodilating effect, due to which the antihypertensive effect of the drug may be enhanced.

A decrease in blood pressure is not accompanied by changes in blood volume, cerebral and renal blood flow, blood supply to internal organs, skeletal muscles, skin, or reflex activity of the myocardium. After oral administration, the hypotensive effect develops within 1 hour, reaches a maximum after 3–6 hours and persists for 24 hours.

In heart failure, the positive effects of Monopril® are achieved mainly through inhibition of the renin-aldosterone system. Suppression of ACE leads to a decrease in both preload and afterload on the myocardium.

The drug helps to increase tolerance to physical activity and reduce the severity of heart failure.

Contraindications

Quincke's edema.
Hypersensitivity to any of the components of the drug.
Age up to 18 years.
Pregnancy or lactation.

Use with caution when:

hyponatremia;
bipolar renal artery stenosis ;
desensitization;
aortic stenosis;
condition after kidney transplantation;
renal failure;
systemic connective tissue lesions;
hemodialysis;
cerebrovascular diseases;
coronary heart disease ; heart failure of the chronic type 3–4 degrees;
diabetes mellitus;
hyperkalemia;
inhibition of hematopoiesis in the bone marrow;
gout;
in old age;
conditions accompanied by a decrease in circulating blood volume.

Pharmacokinetics

After oral administration, absorption is approximately 30–40%. The extent of absorption is independent of food intake, but its rate may be slower. The hydrolytic conversion of fosinopril under the action of enzymes into fosinoprilat occurs mainly in the liver and mucous membrane of the gastrointestinal tract. If liver function is impaired, the rate of hydrolysis may be slowed down, but the degree of conversion does not change noticeably. Cmax in blood plasma is reached after approximately 3 hours and does not depend on the dose taken. Fosinoprilat is ≥95% protein bound, has a relatively small volume of distribution, and is only slightly bound to cellular components of the blood.

Fosinopril is eliminated from the body equally through the liver and kidneys. In patients with arterial hypertension with normal renal and liver function, T1/2 of fosinoprilat is approximately 11.5 hours. In patients with heart failure, the T1/2 value is 14 hours. The clearance of fosinoprilat during hemodialysis and peritoneal dialysis averages 2 and 7%, respectively. in relation to urea clearance values. In patients with impaired renal function (Cl creatinine <80 ml/min/1.73 m2), the total clearance of fosinoprilat from the body is approximately half that of patients with normal renal function, while absorption, bioavailability and protein binding are not noticeably change. Reduced excretion through the kidneys is compensated by increased excretion through the liver. A moderate increase in plasma AUC values (less than double the normal value) is observed in patients with varying degrees of renal failure, including end-stage renal failure (creatinine Cl <10 ml/min/1.73 m2). In patients with impaired liver function (with alcoholic or biliary cirrhosis), the rate of hydrolysis of fosinopril may be reduced, but the degree of hydrolysis does not change noticeably. The total clearance of fosinoprilat from the body of such patients is approximately half that of patients with normal liver function.

Side effects

The most likely side effects of Monopril.

From the circulatory system: chest pain, fainting, orthostatic hypotension , hot flashes, arrhythmia .
Digestive disorders: vomiting, dyspepsia, pancreatitis ALT and AST levels , hepatitis .
From the nervous system: sensory disturbances, feeling of fatigue.
From the genitourinary system: oliguria, proteinuria , increased concentrations of creatinine and urea .
From the respiratory system: sinusitis, pharyngitis , cough, bronchospasm .
From the musculoskeletal system: pain in joints and muscles.
Allergic reactions: photosensitivity , itching , rash , Quincke's edema .

Instructions for use of Monopril (Method and dosage)

Instructions for use of Monopril recommend taking the drug orally. The dosage is selected individually.

Arterial hypertension . The initial dose is 10 mg once a day. It is necessary to select the dose by observing the dynamics of pressure reduction. The standard dose ranges from 11-40 mg once daily. If there is no sufficient hypotensive effect, additional diuretics .

Heart failure . The initial dose is 5 mg up to two times a day. Over time, the dose can be increased to 40 mg per day.

Directions for use and doses

Inside. The dosage of the drug should be selected individually.

Arterial hypertension. The recommended starting dose of the drug is 10 mg once a day. The dose must be selected depending on the dynamics of blood pressure reduction.

The usual dose is 10 to 40 mg once daily. In the absence of a sufficient hypotensive effect, additional diuretics may be prescribed.

If treatment with Monopril® is started against the background of diuretic therapy, then its initial dose should be no more than 10 mg with careful medical monitoring of the patient’s condition.

Heart failure. The recommended starting dose is 5 mg 1 or 2 times a day. Depending on the therapeutic effectiveness, the dose can be increased at weekly intervals up to a maximum of 40 mg once a day.

Arterial hypertension and heart failure with impaired renal or liver function

Since the drug is eliminated from the body in two ways, dose reduction is usually not required for patients with impaired renal or liver function.

Elderly patients. There are no differences in the effectiveness and safety of treatment with the drug in patients aged 65 years and older and in younger patients. However, greater susceptibility to the drug in some elderly patients cannot be ruled out due to possible overdose events due to its slow elimination.

Overdose

Signs: severe decrease in blood pressure, bradycardia, shock , water-mineral imbalance, acute renal failure, stupor.

Therapy: stop taking Monopril, gastric lavage, use of sorbents, vasopressors , intravenous saline, then symptomatic and supportive therapy. Hemodialysis is ineffective.

Monopril tab 20mg No. 28

Compound

The active substance is fosinopril sodium 20 mg.

Pharmacokinetics

Suction and distribution

After oral administration, absorption is approximately 30-40%. The extent of absorption is not influenced by food intake, but its rate may be slowed when the drug is taken with food. Cmax in blood plasma is reached after approximately 3 hours and does not depend on the dose taken. Fosinoprilat is ≥95% bound to blood proteins, has a relatively low Vd and is only slightly bound to cellular components of the blood.

Metabolism and excretion

Enzymatic hydrolysis of fosinopril with the formation of fosinoprilat occurs mainly in the liver and gastrointestinal mucosa. If liver function is impaired, the rate of hydrolysis may be slowed down, but the degree of conversion does not change noticeably.

Fosinoprilat is excreted from the body equally through the intestines with bile and kidneys. In patients with arterial hypertension with normal renal and liver function, T1/2 of fosinoprilat is approximately 11.5 hours.

Pharmacokinetics in special clinical situations

In patients with chronic heart failure, the T1/2 value is 14 hours.

The clearance of fosinoprilat during hemodialysis and peritoneal dialysis averages 2% and 7%, respectively, relative to the clearance values of urea.

In patients with impaired renal function (creatinine clearance less than 80 ml/min/1.73 m2), the total clearance of fosinoprilat is approximately half that of patients with normal renal function. At the same time, absorption, bioavailability and protein binding do not change noticeably. Reduced urinary excretion is compensated by increased intestinal excretion in bile. A moderate increase in plasma AUC (less than double the normal value) is observed in patients with varying degrees of renal failure, including end-stage renal failure (creatinine clearance less than 10 ml/min/1.73 m2).

In patients with impaired liver function (with alcoholic or biliary cirrhosis), the rate of hydrolysis of fosinopril may be reduced, but the degree of hydrolysis does not change noticeably. The total body clearance of fosinoprilat in such patients is approximately half that of patients with normal liver function.

Indications for use

arterial hypertension (monotherapy or in combination with other antihypertensive drugs, in particular thiazide diuretics);
heart failure (as part of combination therapy).

Contraindications

history of hereditary angioedema and idiopathic angioedema (including after taking other ACE inhibitors);
congenital lactose intolerance, lactase deficiency, glucose-galactose malabsorption;
pregnancy;
lactation period (breastfeeding);
age under 18 years (efficacy and safety have not been established);
hypersensitivity to fosinopril or any other substance included in the drug;
history of hypersensitivity to any other ACE inhibitor.

With caution: renal failure; hyponatremia (risk of dehydration, arterial hypotension, chronic renal failure); bilateral renal artery stenosis or stenosis of the artery of a single kidney; aortic stenosis; condition after kidney transplantation; during desensitization; systemic connective tissue diseases (including systemic lupus erythematosus, scleroderma) - increased risk of developing neutropenia or agranulocytosis; during hemodialysis; cerebrovascular diseases (including cerebrovascular insufficiency); IHD; chronic heart failure FC III-IV (NYHA classification); diabetes; inhibition of bone marrow hematopoiesis; hyperkalemia; in elderly patients; gout, following a diet with limited salt; conditions accompanied by a decrease in blood volume (including diarrhea, vomiting, previous treatment with diuretics).

Directions for use and doses

The drug is taken orally. The dose of the drug should be selected individually. For halving, a line is marked on the tablet.

Arterial hypertension

The recommended initial dose of the drug is 10 mg (1/2 tablet of 20 mg) 1 time/day. The dose must be selected depending on the dynamics of blood pressure reduction. The usual dose is from 10 to 40 mg 1 time / day. If there is no sufficient antihypertensive effect, additional diuretics may be prescribed.

If treatment with Monopril is started against the background of diuretic therapy, its initial dose should be no more than 10 mg (1/2 tablet of 20 mg each) with regular medical monitoring of the patient’s condition. The maximum daily dose is 40 mg.

Chronic heart failure

The recommended initial dose of the drug is 10 mg (1/2 tablet of 20 mg) 1 time/day. Treatment begins under mandatory medical supervision. If the initial dose is well tolerated, it can be gradually increased at weekly intervals, up to 40 mg 1 time / day (maximum daily dose). The drug should be prescribed in combination with a diuretic. Concomitant use of digoxin is not necessary.

Since the drug is eliminated from the body in two ways, dose adjustment is usually not required for patients with impaired renal or hepatic function.

There are no differences in the effectiveness and safety of treatment of the drug between patients aged 65 years and older and younger patients, so dose adjustment for elderly patients is usually not required. However, greater susceptibility to the drug in some elderly patients cannot be ruled out, due to possible overdose events due to delayed elimination of the drug.

Storage conditions

The drug should be stored out of the reach of children, in a dry place at a temperature of 15° to 25°C.

Best before date

2 years. Do not use after the expiration date.

special instructions

Before starting treatment, it is necessary to analyze previous antihypertensive therapy, the degree of increase in blood pressure, dietary restrictions on salt and/or liquid, and other clinical circumstances. If possible, previous antihypertensive therapy should be discontinued several days before starting treatment with Monopril.

To reduce the likelihood of arterial hypotension, diuretics should be discontinued 2-3 days before starting treatment with Monopril.

Before starting treatment and during therapy, it is necessary to monitor blood pressure, kidney function, the content of potassium ions, creatinine, urea, electrolyte content and the activity of liver enzymes in the blood.

Angioedema

The development of angioedema of the extremities, face, lips, mucous membranes, tongue, pharynx or larynx has been reported in patients using the drug Monopril. Swelling of the tongue, pharynx, or larynx can cause airway obstruction, which can be fatal. In such cases, it is necessary to stop taking the drug and take emergency measures, including subcutaneous administration of a solution of epinephrine (adrenaline) (1:1000), as well as taking other emergency treatment measures. In most cases, with swelling of the face, oral mucosa, lips and limbs, stopping the drug led to normalization of the condition; however, appropriate therapy was sometimes required.

Swelling of the intestinal mucosa

Swelling of the intestinal mucosa has rarely been observed while taking ACE inhibitors. Patients complained of abdominal pain (there may have been no nausea and vomiting); in some cases, swelling of the intestinal mucosa occurred without swelling of the face; C1-esterase activity was normal. Symptoms disappeared after stopping the use of ACE inhibitors. Edema of the intestinal mucosa should be included in the differential diagnosis of patients taking ACE inhibitors who complain of abdominal pain.

Anaphylactic reactions during dialysis using high-permeability membranes

Anaphylactic reactions can develop in patients taking ACE inhibitors during hemodialysis using high-permeability membranes, as well as during LDL apheresis with adsorption to dextran sulfate. In these cases, the use of a different type of dialysis membrane or the use of a different class of antihypertensive drugs should be considered.

Anaphylactic reactions during desensitization

In two patients, during desensitization with hymenoptera venom while taking the ACE inhibitor enalapril, life-threatening anaphylactoid reactions were noted. In the same patients, these reactions were avoided by timely interruption of the ACE inhibitor; however, they reappeared after inadvertent resumption of an ACE inhibitor. Particular care should be taken when desensitizing patients taking ACE inhibitors.

Neutropenia/agranulocytosis

It is possible to develop agranulocytosis and suppression of bone marrow function during treatment with ACE inhibitors. These cases occur more often in patients with impaired renal function, especially in the presence of systemic connective tissue diseases (systemic lupus erythematosus or scleroderma). Before starting therapy with ACE inhibitors and during treatment, leukocytes and leukocyte formula are determined (once a month in the first 3-6 months of treatment and in the first year of use of the drug in patients with an increased risk of neutropenia).

Arterial hypotension

In patients with uncomplicated arterial hypertension, arterial hypotension may develop due to the use of the drug Monopril.

Symptomatic arterial hypotension when using ACE inhibitors more often develops in patients during intensive treatment with diuretics, a diet associated with limiting sodium chloride, or during dialysis. Transient arterial hypotension is not a contraindication for the use of the drug after measures have been taken to restore blood volume.

In patients with chronic heart failure, treatment with ACE inhibitors may cause excessive antihypertensive effects, which can lead to oliguria or azotemia and, in rare cases, to fatal acute renal failure. Therefore, when treating chronic heart failure with Monopril, it is necessary to carefully monitor patients, especially during the first 2 weeks of treatment, as well as with any increase in the dose of Monopril or a diuretic. It may be necessary to reduce the diuretic dose in patients with normal or low blood pressure, who have previously received diuretic therapy, or who have hyponatremia. Arterial hypotension as such is not a contraindication for further use of the drug Monopril in chronic heart failure.

Some reduction in systemic blood pressure is a common and desirable effect when starting the drug in chronic heart failure. The extent of this reduction is greatest early in treatment and stabilizes within one or two weeks of starting treatment. Blood pressure usually returns to baseline levels without a decrease in therapeutic efficacy.

Liver dysfunction

In rare cases, when using ACE inhibitors, a syndrome is observed, the first manifestation of which is cholestatic jaundice. This is followed by fulminant liver necrosis, sometimes fatal. The mechanism of development of this syndrome has not been studied. If noticeable jaundice appears and a marked increase in the activity of liver enzymes, treatment with Monopril should be discontinued and appropriate treatment should be prescribed.

In patients with impaired liver function, increased plasma concentrations of fosinopril may be observed. In liver cirrhosis (including alcoholic cirrhosis), the apparent total clearance of fosinoprilat is reduced, and the AUC is approximately 2 times higher than in patients without liver dysfunction.

Renal dysfunction

In patients with arterial hypertension with unilateral or bilateral renal artery stenosis or stenosis of the artery of a single kidney, the concentration of blood urea nitrogen and serum creatinine may increase during treatment with ACE inhibitors. These effects are usually reversible and disappear after treatment is stopped. It is necessary to monitor renal function in such patients in the first weeks of treatment. In some patients, increases in blood urea nitrogen and serum creatinine concentrations (usually small and transient) may be observed even without obvious renal impairment when using Monopril and diuretics simultaneously. It may be necessary to reduce the dose of Monopril.

In patients with severe chronic heart failure, renal function may be dependent on the activity of the RAAS, so treatment with ACE inhibitors may be accompanied by oliguria and/or progressive azotemia, and in rare cases, acute renal failure and death.

Hyperkalemia

There have been cases of increased levels of potassium ions in the blood serum of patients taking ACE inhibitors, incl. fosinopril The risk group in this regard includes patients with renal failure, type 1 diabetes mellitus, as well as those taking potassium-sparing diuretics, potassium-containing nutritional supplements or other drugs that increase the content of potassium ions in the blood serum (for example, heparin).

Cough

When using ACE inhibitors, including fosinopril, a non-productive, persistent cough was observed, which disappeared after discontinuation of therapy. When cough occurs in patients taking ACE inhibitors, this therapy should be considered as a possible cause in the differential diagnosis.

Surgery/general anesthesia

ACE inhibitors may enhance the antihypertensive effect of drugs used for general anesthesia. Before surgery (including dentistry), you must warn your doctor/anesthesiologist about the use of ACE inhibitors.

Caution should be exercised when performing physical exercise or in hot weather due to the risk of dehydration and hypotension due to decreased circulating fluid volume.

Description

ACE inhibitor.

Dosage form

The tablets are white or almost white, round, biconvex, practically odorless, scored on one side and engraved “609” on the other side.

Use in children

The use of the drug is contraindicated for people under 18 years of age, because efficacy and safety have not been established.

Action

Fosinopril sodium is chemically the sodium salt of the ester of the pharmacologically active compound fosinoprilat. Once in the human body, fosinopril undergoes enzymatic hydrolysis and turns into fosinoprilat. Fosinoprilat, due to the presence of a phosphinate group, is a specific competitive inhibitor of angiotensin-converting enzyme (ACE). Due to ACE inhibition, fosinoprilat prevents the conversion of angiotensin I to angiotensin II, which has a vasoconstrictor effect. ACE inhibition leads to a decrease in the concentration of angiotensin II in the blood plasma, which causes a decrease in its vasopressor activity and a decrease in aldosterone secretion. Decreased aldosterone secretion may lead to a slight increase in serum potassium ions (average 0.1 mEq/L) and a decrease in sodium ions and fluid volume.

Fosinoprilat slows down the metabolism of bradykinin, which has a powerful vasodilating effect; due to this, its antihypertensive effect is enhanced.

After oral administration, the antihypertensive effect develops within 1 hour, reaches a maximum after 2-6 hours and lasts 24 hours. The antihypertensive effect of the drug is manifested to the same extent in the patient's standing and lying position. Orthostatic hypotension and tachycardia are sometimes observed in patients who are hypovolemic or on a salt-free diet. It may take several weeks to achieve maximum therapeutic effect. The antihypertensive effects of fosinopril and thiazide diuretics complement each other. The effectiveness of the antihypertensive effect does not depend on age, gender and body weight. The drug has no withdrawal syndrome even with abrupt cessation of treatment.

In chronic heart failure, the positive effect of the drug Monopril is achieved mainly through inhibition of the RAAS. Suppression of ACE leads to a decrease in both preload and afterload on the myocardium. The drug helps to increase tolerance to physical activity and reduce the severity of chronic heart failure.

Side effects

From the cardiovascular system: marked decrease in blood pressure, orthostatic hypotension, tachycardia, syncope, arrhythmia, palpitations, angina pectoris, myocardial infarction, flushes of blood to the facial skin, cardiac conduction disturbances, increased blood pressure, sudden death, cardiac arrest, peripheral swelling.

From the urinary system: renal failure, proteinuria, prostate pathology (hyperplasia, adenoma), polyuria, oliguria.

From the nervous system: stroke, cerebral ischemia, dizziness, imbalance, headache, weakness, memory impairment, sleep disturbances, anxiety, depression, confusion, drowsiness, paresthesia.

From the senses: hearing and vision impairment, ear pain, tinnitus, change in taste.

From the digestive system: nausea, diarrhea, intestinal obstruction, pancreatitis, hepatitis, cholestatic jaundice, abdominal pain, vomiting, constipation, anorexia, stomatitis, glossitis, dysphagia, flatulence, loss of appetite, dry oral mucosa, bleeding.

From the respiratory system: pneumonia, dry cough, pulmonary infiltrates, bronchospasm, shortness of breath, rhinorrhea, sinusitis, laryngitis, pharyngitis, tracheobronchitis, dysphonia, nosebleeds. Two patients had a symptom complex: bronchospasm, cough, eosinophilia.

From the circulatory and lymphatic system: inflammation of the lymph nodes.

From the musculoskeletal system: arthritis, myalgia, musculoskeletal pain, muscle weakness in the extremities.

Metabolism: exacerbation of gout.

Allergic reactions: skin rash, itching, angioedema, dermatitis.

Other: increased body temperature, hyperhidrosis, sexual dysfunction, changes in body weight.

From laboratory parameters: hypercreatininemia, increased urea content, increased activity of liver enzymes, hyperbilirubinemia, hyperkalemia, hyponatremia, decreased hemoglobin and hematocrit, increased ESR, leukopenia, neutropenia, eosinophilia.

Effect on the fetus: impaired development of the fetal kidneys, decreased blood pressure in the fetus and newborns, impaired renal function, hyperkalemia, hypoplasia of the skull bones, oligohydramnios, contracture of the limbs, pulmonary hypoplasia.

Use during pregnancy and breastfeeding

Monopril is contraindicated during pregnancy. The use of ACE inhibitors during pregnancy can cause developmental disorders or fetal death. If pregnancy is detected during treatment with Monopril, it should be stopped as soon as possible. If (in rare cases) there is no alternative to ACE inhibitors for treatment of the patient, she should be informed about the potential harm of treatment to the development of the fetus and a thorough ultrasound examination should be performed to identify fetal pathology. If oligohydramnios is detected, treatment with Monopril is not canceled only if it is carried out for health reasons. It should be kept in mind that oligohydramnios is sometimes detected only when there is irreversible damage to the fetus.

Arterial hypotension, oliguria, and hyperkalemia were observed in newborns whose mothers took ACE inhibitors during pregnancy.

Infants whose mothers took ACE inhibitors during pregnancy should be carefully monitored for hypotension, oliguria, and hyperkalemia. If a newborn has oliguria, efforts should be made to control blood pressure and support renal perfusion. Exchange transfusion or dialysis may be necessary to restore blood pressure and replace impaired renal function. Fosinopril is slowly eliminated from the circulating blood in adults during hemodialysis and peritoneal dialysis. There is no experience with the removal of fosinopril from the circulating blood in newborns.

Since fosinopril is found in breast milk, the drug should not be used during breastfeeding.

Interaction

Concomitant use of antacids (for example, aluminum or magnesium hydroxide) and the carminative simethicone may reduce the absorption of fosinopril. Therefore, these products must be used at intervals of at least 2 hours.

With the simultaneous use of ACE inhibitors with lithium salts, the lithium content in the blood serum and the risk of developing lithium intoxication may increase, so Monopril and lithium preparations should be used simultaneously with caution. Careful monitoring of serum lithium levels is recommended.

It is known that indomethacin can reduce the antihypertensive effect of ACE inhibitors, especially in patients with arterial hypertension and low plasma renin activity. Other NSAIDs, for example, acetylsalicylic acid, and selective COX-2 inhibitors can have a similar effect. In patients over 65 years of age, with hypovolemia (including during treatment with diuretics), with impaired renal function, simultaneous administration of NSAIDs, including selective COX-2 inhibitors and ACE inhibitors (including fosinopril) may lead to deterioration of function kidneys, up to acute renal failure. Usually this condition is reversible. Renal function should be carefully monitored in patients taking fosinopril and NSAIDs. With the simultaneous use of Monopril with diuretics, especially at the beginning of diuretic therapy, as well as in combination with a strict diet limiting the intake of table salt, or with dialysis, a pronounced decrease in blood pressure may develop, especially in the first hour after taking the initial dose of Monopril.

Potassium supplements and potassium-sparing diuretics (amiloride, spironolactone, triamterene) increase the risk of developing hyperkalemia. In patients with heart failure, diabetes mellitus, and concomitantly taking potassium-sparing diuretics, potassium-containing salt substitutes, or other drugs that cause hyperkalemia (for example, heparin), ACE inhibitors increase the risk of an increase in the content of potassium ions in the blood serum.

Fosinopril enhances the hypoglycemic effect of sulfonylurea derivatives, insulin, and the risk of developing leukopenia when used simultaneously with allopurinol, cytostatic agents, immunosuppressants, procainamide.

Estrogens weaken the antihypertensive effect of Monopril due to their ability to retain water.

Antihypertensive drugs, narcotic analgesics, drugs for general anesthesia enhance the antihypertensive effect of Monopril.

The bioavailability of the drug does not change when used simultaneously with chlorthalidone, nifedipine, propranolol, hydrochlorothiazide, cimetidine, metoclopramide, propantheline bromide, digoxin and warfarin.

Overdose

Symptoms: marked decrease in blood pressure, bradycardia, shock, water and electrolyte imbalance, acute renal failure, stupor.

Treatment: the drug should be stopped, gastric lavage, sorbents (for example, activated carbon), vasodepressants, infusion of 0.9% sodium chloride solution, and then symptomatic and supportive treatment are indicated. The use of hemodialysis is ineffective.

Impact on the ability to drive vehicles and operate machinery

Care must be taken when driving vehicles or performing other work that requires increased attention, because Dizziness may occur.

Interaction

Concomitant use with antacids reduces the absorption of fosinopril , so they should be taken at intervals of 2 hours.

When used together with lithium salts, lithium intoxication increases .

Nonsteroidal anti-inflammatory drugs suppress the antihypertensive effect of Monopril and similar drugs.

When using the drug simultaneously with diuretics, an excessive decrease in blood pressure may develop.

Drugs containing potassium and potassium-sparing diuretics increase the likelihood of developing hyperkalemia .

Fosinopril activates the hypoglycemic effect of insulin and sulfonylurea ; increases the risk of leukopenia when used with cytostatic agents, immunosuppressants, Allopurinol, Procainamide.

Estrogens suppress the antihypertensive effect of Monopril.

special instructions

If possible, previous antihypertensive treatment should be discontinued several days before starting treatment with Monopril®.

To reduce the likelihood of arterial hypotension, diuretics should be discontinued 2-3 days before starting treatment with Monopril®.

Before and during treatment, it is necessary to monitor blood pressure, renal function, the content of potassium ions, creatinine, urea, electrolyte concentrations and the activity of liver enzymes in the blood.

Angioedema. The development of angioedema has been reported in patients using Monopril®. Swelling of the tongue, pharynx, or larynx can cause airway obstruction, which can be fatal. If such reactions develop, it is necessary to stop taking the drug and subcutaneously administer a solution of epinephrine (adrenaline) (1:1000), as well as take other emergency treatment measures.

Swelling of the intestinal mucosa. Swelling of the intestinal mucosa has rarely been observed while taking ACE inhibitors. These patients complained of abdominal pain (there may have been no nausea and vomiting), in some cases swelling of the intestinal mucosa occurred without swelling of the face, and the level of C1-esterases was normal. Symptoms disappeared after stopping the use of ACE inhibitors. Edema of the intestinal mucosa should be included in the differential diagnosis of patients taking ACE inhibitors who complain of abdominal pain.

Anaphylactic reactions during dialysis using high-permeability membranes can develop in patients who used ACE inhibitors during hemodialysis through high-permeability membranes, as well as during apheresis of low-density lipoproteins with adsorption to dextran sulfate. In these cases, the use of a different type of dialysis membrane or other antihypertensive treatment should be considered.

Neutropenia/agranulocytosis. It is possible to develop agranulocytosis and suppression of bone marrow function during treatment with ACE inhibitors. These cases occur more often in patients with impaired renal function, especially in the presence of systemic connective tissue diseases (systemic lupus erythematosus or scleroderma). Before starting therapy with ACE inhibitors and during treatment, the total number of leukocytes and the leukocyte formula are determined (once a month in the first 3-6 months of treatment and in the first year of using the drug in patients with an increased risk of neutropenia).

Arterial hypotension. In patients with uncomplicated arterial hypertension, arterial hypotension may develop due to the use of the drug Monopril®.

Symptomatic hypotension with the use of ACE inhibitors most often develops in patients after intensive treatment with diuretics, a salt-restricted diet, or during renal dialysis. Temporary arterial hypotension is not a contraindication for the use of the drug after taking measures to hydrate the body.

In patients with chronic heart failure, treatment with ACE inhibitors may cause excessive antihypertensive effects, which can lead to oliguria or azotemia, which can be fatal. Therefore, when treating chronic heart failure with Monopril®, it is necessary to carefully monitor patients, especially during the first 2 weeks of treatment, as well as with any increase in the dose of Monopril® or a diuretic.

A reduction in the diuretic dose may be required in patients with hyponatremia and in patients previously intensively treated with diuretics. Arterial hypotension is not a contraindication for further use of the drug Monopril®. Some reduction in systemic blood pressure is a common and desirable effect when starting the drug for heart failure. The extent of this reduction is greatest early in treatment and stabilizes within one or two weeks of starting treatment. Blood pressure usually returns to pre-treatment values without a decrease in therapeutic efficacy.

Liver dysfunction. If noticeable jaundice appears and a marked increase in the activity of liver enzymes, treatment with Monopril® should be discontinued and appropriate treatment should be prescribed.

Renal dysfunction. In patients with arterial hypertension with bilateral renal artery stenosis or stenosis of the artery of a single kidney, as well as with the simultaneous use of diuretics without signs of renal vascular disease, the concentration of blood urea nitrogen and serum creatinine may increase during treatment with ACE inhibitors. These effects are usually reversible and disappear after treatment is stopped. It may be necessary to reduce the dose of diuretic and/or Monopril®.

In patients with severe chronic heart failure, with altered activity of the renin-angiotensin-aldosterone system, treatment with ACE inhibitors can lead to oliguria, progressive azotemia and, in rare cases, acute renal failure and possible death.

Surgical interventions/general anesthesia. ACE inhibitors may enhance the hypotensive effect of drugs used for general anesthesia. Before surgery (including dentistry), you must warn your doctor about the use of ACE inhibitors.

Monopril® is contraindicated during pregnancy. The use of ACE inhibitors during the second and third trimesters of pregnancy causes damage or even death to the developing fetus. Since fosinopril is found in breast milk, the drug should not be used during breastfeeding. For newborns whose mothers took ACE inhibitors during pregnancy, it is recommended to carefully monitor them for timely detection of arterial hypotension, oliguria and hyperkalemia.

Caution should be exercised when driving or performing other work requiring increased alertness, as dizziness may occur, especially after the initial dose of an ACE inhibitor in patients taking diuretics. Caution should be exercised when performing physical exercise or in hot weather due to the risk of dehydration and hypotension due to decreased circulating fluid volume.

Analogues of Monopril

Level 4 ATC code matches:
Dilaprel

Prenesa

Enap

Diroton

Lipril

Renipril

Parnavel

Fozinap

Tritace

Enam

Zokardis

Fosinopril

Lisinopril

Captopril

Renitek

Hartil

Phosicard

Amprilan

Ramipril

Perindopril

The most common analogues of Monopril: Fosicard , Fosinap, Fozinotec, Fosinopril-Teva.

Monopril price, where to buy

The price of Monopril 20 mg No. 28 in Russia fluctuates around 309-430 rubles, in Ukraine – 173-273 hryvnia.

Online pharmacies in RussiaRussia

ZdravCity

Monopril tablets 20mg 28 pcs.Bristol Myers Squibb CpL/ICN Polfa Rzeszow SA
RUR 508 order